ArticleJournal of virology2001
Identification of a novel element involved in regulation of the lytic switch BZLF1 gene promoter of Epstein-Barr virus.
Article in Journal of virology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Pooled it
- Locus-specific proteomics identifies novel regulators of Epstein-Barr virus lytic reactivation.Journal of virology · 2026Article
- Reactivation of Epstein-Barr Virus by HIF-1α Requires p53.Journal of virology · 2020Article
- Serological Assessment of 18 Pathogens and Risk of AIDS-Associated Non-Hodgkin Lymphoma.Journal of acquired immune deficiency syndromes (1999) · 2019Article
- Cellular differentiation regulator BLIMP1 induces Epstein-Barr virus lytic reactivation in epithelial and B cells by activating transcription from both the R and Z promoters.Journal of virology · 2015Article
- Activation and repression of Epstein-Barr Virus and Kaposi's sarcoma-associated herpesvirus lytic cycles by short- and medium-chain fatty acids.Journal of virology · 2014Article
- The pathogenesis of Epstein-Barr virus persistent infection.Current opinion in virology · 2013Review
- The cycle of EBV infection explains persistence, the sizes of the infected cell populations and which come under CTL regulation.PLoS pathogens · 2013Article
- Shutoff of BZLF1 gene expression is necessary for immortalization of primary B cells by Epstein-Barr virus.Journal of virology · 2012Article
- Transforming growth factor beta-induced reactivation of Epstein-Barr virus involves multiple Smad-binding elements cooperatively activating expression of the latent-lytic switch BZLF1 gene.Journal of virology · 2011Article
- The ZIIR element of the Epstein-Barr virus BZLF1 promoter plays a central role in establishment and maintenance of viral latency.Journal of virology · 2011Article
- Cellular microRNAs 200b and 429 regulate the Epstein-Barr virus switch between latency and lytic replication.Journal of virology · 2010Article
- Either ZEB1 or ZEB2/SIP1 can play a central role in regulating the Epstein-Barr virus latent-lytic switch in a cell-type-specific manner.Journal of virology · 2010Article
- ZEB1 regulates the latent-lytic switch in infection by Epstein-Barr virus.PLoS pathogens · 2007Article
- ZEB1 and c-Jun levels contribute to the establishment of highly lytic Epstein-Barr virus infection in gastric AGS cells.Journal of virology · 2007Article
- Contribution of C/EBP proteins to Epstein-Barr virus lytic gene expression and replication in epithelial cells.Journal of virology · 2006Article
- Lytic cycle gene regulation of Epstein-Barr virus.Journal of virology · 2004Article
- Postinternalization inhibition of adenovirus gene expression and infectious virus production in human T-cell lines.Journal of virology · 2004Article
- Article
- Virally targeted therapies for EBV-associated malignancies.Oncogene · 2003Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Epstein-Barr virus (EBV) is a human herpesvirus capable of establishing a latent state in B lymphocytes. EBV's BZLF1 gene product plays a central role in regulating the switch from latency to productive infection. Here, we identify a sequence element, 5'-CAGGTA-3', called ZV, located at nucleotides -17 to -12 relative to the transcription initiation site of the BZLF1 promoter. ZV sequence-specifically binds a cellular nuclear factor(s), ZVR. ZVR DNA-binding activity was present in the EBV-negative B-lymphocytic cell line DG75, the EBV-positive B-lymphocytic cell lines GG68 and 721, the cervical cell line C33A, and the kidney cell line CV-1 but not in the breast carcinoma cell line MCF-7. Mutations in ZV that relieve binding of ZVR lead to a two- to fourfold increase in basal expression of the BZLF1 promoter in DG75, C33A, and CV-1 cells. The same mutants exhibited a 40- to 180-fold increase in tetradecanoyl phorbol acetate-ionomycin-induced expression in DG75 cells and a 22-fold increase in C33A cells. Thus, ZVR functions as a regulator of the BZLF1 promoter, repressing transcription when bound to the ZV site in the absence of inducers. No differences in basal or induced transcription between wild-type and ZV mutant BZLF1 promoters were observed in ZVR-negative MCF-7 cells. ZVR failed to bind any of the previously identified negative regulatory elements within the BZLF1 promoter. We conclude that ZV functions as an important regulatory element of the BZLF1 promoter, with ZVR likely playing important roles in the maintenance of latency and reactivation of EBV.
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Registered trials
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